Granata A R
Gen Pharmacol. 1985;16(5):463-8. doi: 10.1016/0306-3623(85)90005-9.
In the isolated perfused mesenteric arteries of the rat, neither (+/-) propranolol (0.1 microM) nor (+/-)isoproterenol (0.05 microM) modified the overflow of DL-[3H]noradrenaline (DL-[3H]NA) induced by sympathetic nerve stimulation at either 5 or 10 Hz. The blockade of alpha presynaptic receptors with phentolamine (4.7 microM) increased the 3H-transmitter overflow at 5 and 10 Hz. (+/-)Propranolol (0.1 microM) failed to modify this effect. Vasoconstrictor responses to exogenous NA or sympathetic nerve stimulation were not modified by (+/-)propranolol (0.1 microM). Prolonged treatment with (+/-)propranolol (7 mg/kg) for 15 days potentiates responses to both exogenous NA and sympathetic nerve stimulation; however, the fractional release per pulse of DL-[3H]NA was not modified at either 5 or 10 Hz. These results provide no evidence to support the hypothesis that the release of NA is regulated by presynaptic beta-adrenoreceptors in the mesenteric arteries of the rat. The enhancement of vascular responses after prolonged treatment with propranolol could be caused by postsynaptic supersensitivity.
在大鼠离体灌注的肠系膜动脉中，无论是（±）普萘洛尔（0.1微摩尔）还是（±）异丙肾上腺素（0.05微摩尔），都不会改变在5赫兹或10赫兹交感神经刺激诱导下的DL-[3H]去甲肾上腺素（DL-[3H]NA）溢出。用酚妥拉明（4.7微摩尔）阻断α突触前受体可增加5赫兹和10赫兹时的3H递质溢出。（±）普萘洛尔（0.1微摩尔）未能改变这种效应。（±）普萘洛尔（0.1微摩尔）对外源性去甲肾上腺素或交感神经刺激引起的血管收缩反应没有影响。用（±）普萘洛尔（7毫克/千克）长期治疗15天可增强对外源性去甲肾上腺素和交感神经刺激的反应；然而，在5赫兹或10赫兹时，每个脉冲的DL-[3H]NA分数释放没有改变。这些结果没有提供证据支持去甲肾上腺素的释放受大鼠肠系膜动脉突触前β-肾上腺素能受体调节的假说。长期用普萘洛尔治疗后血管反应的增强可能是由突触后超敏反应引起的。
